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• Renal allograft rejection.

• Cavernous haemangioma.

• Aortic aneurysm.

• Transfusion reaction.

Cardiopulmonary bypass surgery—abnormal platelet function and thrombocytopenia are frequently seen in patients subjected to cardiopulmonary bypass surgery. Impaired aggregation studies in vitro occur in proportion to duration of the bypass procedure. Believed due to platelet activation and fragmentation in the extracorporeal loop. Platelet transfusion is required in patients with a prolonged bleeding time and excessive haemorrhage after cardiopulmonary bypass surgery.

DIC—platelet exhaustion due to an acquired storage pool defect may occur in DIC due to in vivo platelet stimulation and this may cause abnormal platelet aggregation in in vitro tests. However, haemorrhage in DIC is multifactorial (ffl p512).

Dysproteinaemias—binding of M-proteins to platelet cell membranes in myeloma (particularly IgA) or Waldenstrom's macroglobulinaemia may result in acquired platelet function defects and less commonly clinical bleeding. Severity of platelet function defect correlates with M-protein concentration. Note: haemorrhage is more commonly due to 380 thrombocytopenia or hyperviscosity. Plasmapheresis to remove circulating M-protein may be necessary in bleeding patient in whom the M-protein may be contributory factor through hyperviscosity or impairment of platelet function.

Antiplatelet antibodies—impaired platelet function may be a rare consequence of binding of IgM or IgG molecules to platelet membrane in ITP, SLE and platelet alloimmunisation where the most common result is accelerated platelet destruction and thrombocytopenia. May result in haemorrhagic manifestations at unexpectedly high platelet counts, and in longer than expected bleeding time. If bleeding occurs treatment is that of ITP (M p388).

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